The present study was nndertaken to evaluate the effect of Contagious Skin Necrosis (CSN) with or without tiypanosomosis on blood oxidative status in camels. A total of 15 camels were subjected to the study. Out of them, 10 camels were suffered from CSN. Sterile bacteriological swabs from skin necrosed area whole blood samples for hematological analysis and for diagnosis of trypanosomosis and sennn samples for measuring lipid peroxidation product (Malondialdehyde) were collected. The bacteriological examination revealed that Staphylococcus aureus was the predominant bacterial isolate alone in 6 cases and coupled with other bacteria in the remained 4 cases, the latter was coupled with coagulase negative staphylococci in 3 cases and coupled with Streptococcus agalactiae in one case. Trypanosoma evansi infection was identified using polymerase chain reaction in 5 camels that had CSN. Malondialdehyde showed significant increase in camels affected with CSN that associated with trypanosomosis. The cment study revealed that Staphylococcus aureus was the predominant bacterial isolate in camels with CSN. Lipid peroxidation products increased in the blood of camels with CSN that associated with trypanosomosis, It is recommended to supply camels suffering from CSN with antioxidants to overcome the deterioration of blood oxidative status.

The present study was nndertaken to evaluate the effect of Contagious Skin Necrosis (CSN) with or without tiypanosomosis on blood oxidative status in camels. A total of 15 camels were subjected to the study. Out of them, 10 camels were suffered from CSN. Sterile bacteriological swabs from skin necrosed area whole blood samples for hematological analysis and for diagnosis of trypanosomosis and sennn samples for measuring lipid peroxidation product (Malondialdehyde) were collected. The bacteriological examination revealed that Staphylococcus aureus was the predominant bacterial isolate alone in 6 cases and coupled with other bacteria in the remained 4 cases, the latter was coupled with coagulase negative staphylococci in 3 cases and coupled with Streptococcus agalactiae in one case. Trypanosoma evansi infection was identified using polymerase chain reaction in 5 camels that had CSN. Malondialdehyde showed significant increase in camels affected with CSN that associated with trypanosomosis. The cment study revealed that Staphylococcus aureus was the predominant bacterial isolate in camels with CSN. Lipid peroxidation products increased in the blood of camels with CSN that associated with trypanosomosis, It is recommended to supply camels suffering from CSN with antioxidants to overcome the deterioration of blood oxidative status.

In this study we compared the effect of dinoprost and cloprostenol on changes of corpus luteum blood flow during luteolysis. Ten nonlactating cyclic ewes were synchronized with double PGF2α injections 11 days apart. At Day 10, the animals were classified into 2 groups and received the third dose of PGF2α after confirmation of the presence of a mature CL. The first group received (12.5 mg/im) dinoprost and the second group received (250 μg/im) cloprostenol. A color Doppler ultrasound scan was performed by the same operator according to the following timeline: 0, 0.5, 1, 2, 4, 6, 12, and 24 hours, then every 24 hours until Day 4). The size, morphology, and blood flow of the CL was evaluated during the regression. The results showed that regression of the CL did not differ between the dinoprost and cloprostenol groups. There was no significant effect on diameter of the CL in both groups, though the size of the CL decreased gradually and slowly. Pretreatment progesterone concentration did not differ between groups. The results showed that the nitric oxide level was significantly increased within half an hour after the dinoprost treatment, and was significantly decreased in the cloprostenol group after half an hour. The blood velocity was increased significantly half an hour after the dinoprost treatment and it was decreased in the cloprostenol-treated group. In conclusion, both cloprostenol and dinoprost affect CL by controlling the nitric oxide level and blood supply of the CL via different mechanisms to induce luteolysis.